COVID-19患者高凝血症的负担

M. Kim, A. George, L. Ganti, Derrick Huang, Matthew Carman
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引用次数: 3

摘要

新型冠状病毒病2019 (COVID-19)感染对多器官系统产生广泛影响,包括内皮细胞损伤。各种研究已经发现了严重急性呼吸综合征-冠状病毒-2 (SARS-CoV-2)与内皮细胞之间相互作用导致后者广泛损伤的直接机制的证据,以及间接机制,如过度升高的细胞因子,也可导致相同的结果。内皮的损伤导致血栓形成因子的释放和纤维蛋白溶解的抑制。这给感染或从COVID-19感染中恢复的患者带来了严重的高凝负担。在本病例报告中,作者报告了在最近感染COVID-19的情况下,一位先生出现广泛的深静脉血栓形成和肺栓塞的病例。讨论了假定的机制和管理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Burden of Hypercoagulability in COVID-19
The novel coronavirus disease 2019 (COVID-19) infection has widespread impact on multiple organ systems, including damage to endothelial cells. Various studies have found evidence for direct mechanisms by which interaction between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) and endothelial cells lead to extensive damage to the latter, and indirect mechanisms, such as excessively elevated cytokines, can also result in the same outcome. Damage to the endothelium results in release of thrombotic factors and inhibition of fibrinolysis. This confers a significant hypercoagulability burden on patients infected or recovering from COVID-19 infection. In this case report, the authors report the case of a gentleman presenting with extensive deep vein thrombosis and pulmonary embolism, in the context of recent COVID-19 infection. The postulated mechanisms and management are discussed.
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